Prevailing evidence establishes the influence of an infant’s gut microbiota on immune responses and associated intestinal disorders. The role of functional programming of effector immune cells at extra-intestinal mucosal sites, particularly the lung, is increasing in interest. Animal and human studies show that microbial ligands and metabolites produced by the gut microbiome shape respiratory immunity, while lung directed insults, in turn, influence gut microbiome function. Common connections between development of gut and lung microbiomes and reciprocal signaling between the two organ systems has reinforced the concept of a gut-lung axis. In that context, this review evaluates the mechanistic evidence associating preterm acute lung injury to the development of necrotizing enterocolitis, and subsequently, to the progression to chronic lung disease or bronchopulmonary dysplasia. By focusing on mediators involved in this gut-lung crosstalk, we seek to highlight avenues to prevent or reduce the severity of two of the major morbidities of prematurity.
Jawale et al. (2026) studied this question.